Editing Pseudoephedrine (section)

==Pharmacology==
===Pharmacodynamics===
Pseudoephedrine is a [[sympathomimetic|sympathomimetic agent]] which acts primarily or exclusively by [[norepinephrine releasing agent|inducing the release of norepinephrine]].<ref name="Abraham2003">{{cite book | vauthors = Abraham DJ | title=Burger's Medicinal Chemistry and Drug Discovery | publisher=Wiley | date=15 January 2003 | isbn=978-0-471-26694-5 | doi=10.1002/0471266949.bmc093 | page=}}</ref><ref name="ODonnell1995">{{cite journal | vauthors = O'Donnell SR | title = Sympathomimetic vasoconstrictors as nasal decongestants | journal = Med J Aust | volume = 162 | issue = 5 | pages = 264–267 | date = March 1995 | pmid = 7534374 | doi = 10.5694/j.1326-5377.1995.tb139882.x | url = }}</ref><ref name="Eccles2007" /><ref name="RothmanVuPartilla2003" /> Hence, it is an indirectly acting sympathomimetic.<ref name="Abraham2003" /><ref name="ODonnell1995" /><ref name="Eccles2007" /> Some sources state that pseudoephedrine has a mixed [[mechanism of action]] consisting of both indirect and direct effects by binding to and acting as an [[agonist]] of [[adrenergic receptor]]s.<ref name="GłowackaWiela-Hojeńska2021" /><ref name="VanBerkelFuller2015" /> However, the [[affinity (pharmacology)|affinity]] of pseudoephedrine for adrenergic receptors is described as very low or negligible.<ref name="Abraham2003" /> [[Animal study|Animal studies]] suggest that the sympathomimetic effects of pseudoephedrine are exclusively due to norepinephrine release.<ref name="GadAzabKhattab2021">{{cite journal | vauthors = Gad MZ, Azab SS, Khattab AR, Farag MA | title = Over a century since ephedrine discovery: an updated revisit to its pharmacological aspects, functionality and toxicity in comparison to its herbal extracts | journal = Food Funct | volume = 12 | issue = 20 | pages = 9563–9582 | date = October 2021 | pmid = 34533553 | doi = 10.1039/d1fo02093e | url = }}</ref><ref name="KobayashiEndouSakuraya2003">{{cite journal | vauthors = Kobayashi S, Endou M, Sakuraya F, Matsuda N, Zhang XH, Azuma M, Echigo N, Kemmotsu O, Hattori Y, Gando S | title = The sympathomimetic actions of l-ephedrine and d-pseudoephedrine: direct receptor activation or norepinephrine release? | journal = Anesth Analg | volume = 97 | issue = 5 | pages = 1239–1245 | date = November 2003 | pmid = 14570629 | doi = 10.1213/01.ANE.0000092917.96558.3C | url = }}</ref>

{| class="wikitable sortable floatright" style="font-size:small;"
|+ Monoamine release by pseudoephedrine and related agents ({{Abbrlink|EC<sub>50</sub>|half maximal effective concentration}}, nM)<ref name="RothmanBaumann2003">{{cite journal | vauthors = Rothman RB, Baumann MH | title = Monoamine transporters and psychostimulant drugs | journal = Eur. J. Pharmacol. | volume = 479 | issue = 1–3 | pages = 23–40 | year = 2003 | pmid = 14612135 | doi = 10.1016/j.ejphar.2003.08.054}}</ref><ref name="RothmanBaumann2006" />
|-
! Compound !! data-sort-type="number" | {{abbrlink|NE|Norepinephrine}} !! data-sort-type="number" | {{abbrlink|DA|Dopamine}} !! data-sort-type="number" | {{abbrlink|5-HT|Serotonin}} !! Ref
|-
| [[Dextroamphetamine]] (''S''(+)-amphetamine) || 6.6–7.2 || 5.8–24.8 || 698–1765 || <ref name="RothmanBaumannDersch2001">{{cite journal | vauthors = Rothman RB, Baumann MH, Dersch CM, Romero DV, Rice KC, Carroll FI, Partilla JS | title = Amphetamine-type central nervous system stimulants release norepinephrine more potently than they release dopamine and serotonin | journal = Synapse | volume = 39 | issue = 1 | pages = 32–41 | date = January 2001 | pmid = 11071707 | doi = 10.1002/1098-2396(20010101)39:1<32::AID-SYN5>3.0.CO;2-3 | url = }}</ref><ref name="BaumannPartillaLehner2013">{{cite journal | vauthors = Baumann MH, Partilla JS, Lehner KR, Thorndike EB, Hoffman AF, Holy M, Rothman RB, Goldberg SR, Lupica CR, Sitte HH, Brandt SD, Tella SR, Cozzi NV, Schindler CW | title = Powerful cocaine-like actions of 3,4-methylenedioxypyrovalerone (MDPV), a principal constituent of psychoactive 'bath salts' products | journal = Neuropsychopharmacology | volume = 38 | issue = 4 | pages = 552–562 | year = 2013 | pmid = 23072836 | pmc = 3572453 | doi = 10.1038/npp.2012.204 }}</ref>
|-
| [[Cathinone|''S''(–)-Cathinone]] || 12.4 || 18.5 || 2366 || <ref name="RothmanVuPartilla2003" />
|-
| [[Ephedrine]] ((–)-ephedrine) || 43.1–72.4 || 236–1350 || >10000 || <ref name="RothmanBaumannDersch2001" />
|-
| (+)-Ephedrine || 218 || 2104 || >10000 || <ref name="RothmanBaumannDersch2001" /><ref name="RothmanVuPartilla2003" />
|-
| [[Dextromethamphetamine]] (''S''(+)-methamphetamine) || 12.3–13.8 || 8.5–24.5 || 736–1291.7 || <ref name="RothmanBaumannDersch2001" /><ref name="BaumannAyestasPartilla2012">{{cite journal | vauthors = Baumann MH, Ayestas MA, Partilla JS, Sink JR, Shulgin AT, Daley PF, Brandt SD, Rothman RB, Ruoho AE, Cozzi NV | title = The designer methcathinone analogs, mephedrone and methylone, are substrates for monoamine transporters in brain tissue | journal = Neuropsychopharmacology | volume = 37 | issue = 5 | pages = 1192–203 | date = April 2012 | pmid = 22169943 | pmc = 3306880 | doi = 10.1038/npp.2011.304 | url = }}</ref>
|-
| [[Levomethamphetamine]] (''R''(–)-methamphetamine) || 28.5 || 416 || 4640 || <ref name="RothmanBaumannDersch2001" />
|-
| [[Phenylpropanolamine|(+)-Phenylpropanolamine]] ((+)-norephedrine) || 42.1 || 302 || >10000 || <ref name="RothmanVuPartilla2003" />
|-
| [[Phenylpropanolamine|(–)-Phenylpropanolamine]] ((–)-norephedrine) || 137 || 1371 || >10000 || <ref name="RothmanVuPartilla2003" />
|-
| [[Cathine]] ((+)-norpseudoephedrine) || 15.0 || 68.3 || >10000 || <ref name="RothmanVuPartilla2003" />
|-
| [[L-Norpseudoephedrine|(–)-Norpseudoephedrine]] || 30.1 || 294 || >10000 || <ref name="RothmanVuPartilla2003" />
|-
| (–)-Pseudoephedrine || 4092 || 9125 || >10000 || <ref name="RothmanVuPartilla2003" />
|-
| Pseudoephedrine ((+)-pseudoephedrine) || 224 || 1988 || >10000 || <ref name="RothmanVuPartilla2003" />
|-
| colspan="7" style="width: 1px; background-color:#eaecf0; text-align: center;" | '''Notes:''' The smaller the value, the more strongly the substance releases the neurotransmitter. See also [[Monoamine releasing agent#Activity profiles|Monoamine releasing agent § Activity profiles]] for a larger table with more compounds.
|-
|}

Pseudoephedrine [[monoamine releasing agent|induces monoamine release]] ''[[in vitro]]'' with an {{Abbrlink|EC<sub>50</sub>|half maximal effective concentration}} of 224{{nbsp}}nM for [[norepinephrine]] and 1,988{{nbsp}}nM for [[dopamine]], whereas it is inactive for [[serotonin]].<ref name="RothmanVuPartilla2003">{{cite journal | vauthors = Rothman RB, Vu N, Partilla JS, Roth BL, Hufeisen SJ, Compton-Toth BA, Birkes J, Young R, Glennon RA | title = In vitro characterization of ephedrine-related stereoisomers at biogenic amine transporters and the receptorome reveals selective actions as norepinephrine transporter substrates | journal = J Pharmacol Exp Ther | volume = 307 | issue = 1 | pages = 138–145 | date = October 2003 | pmid = 12954796 | doi = 10.1124/jpet.103.053975 | url = }}</ref><ref name="RothmanBaumann2005">{{cite journal | vauthors = Rothman RB, Baumann MH | title = Targeted screening for biogenic amine transporters: potential applications for natural products | journal = Life Sci | volume = 78 | issue = 5 | pages = 512–518 | date = December 2005 | pmid = 16202429 | doi = 10.1016/j.lfs.2005.09.001 | url = }}</ref><ref name="RothmanBaumann2006">{{cite journal | vauthors = Rothman RB, Baumann MH | title = Therapeutic potential of monoamine transporter substrates | journal = Curr Top Med Chem | volume = 6 | issue = 17 | pages = 1845–1859 | date = 2006 | pmid = 17017961 | doi = 10.2174/156802606778249766 | url = }}</ref> As such, it is about 9-fold [[binding selectivity|selective]] for induction of norepinephrine release over dopamine release.<ref name="RothmanVuPartilla2003" /><ref name="RothmanBaumann2005" /><ref name="RothmanBaumann2006" /> The drug has negligible agonistic activity at the [[α1-adrenergic receptor|α<sub>1</sub>-]] and [[α2-adrenergic receptor|α<sub>2</sub>-adrenergic receptor]]s (K<sub>act</sub> >10,000{{nbsp}}nM).<ref name="RothmanVuPartilla2003" /> At the [[β1-adrenergic receptor|β<sub>1</sub>-]] and [[β2-adrenergic receptor|β<sub>2</sub>-adrenergic receptor]]s, it acts as a [[partial agonist]] with relatively low [[affinity (pharmacology)|affinity]] (β<sub>1</sub> = K<sub>act</sub> = 309{{nbsp}}μM, {{Abbrlink|IA|intrinsic activity}} = 53%; β<sub>2</sub> = 10{{nbsp}}μM; {{Abbr|IA|intrinsic activity}} = 47%).<ref name="VansalFeller1999">{{cite journal | vauthors = Vansal SS, Feller DR | title = Direct effects of ephedrine isomers on human beta-adrenergic receptor subtypes | journal = Biochem Pharmacol | volume = 58 | issue = 5 | pages = 807–810 | date = September 1999 | pmid = 10449190 | doi = 10.1016/s0006-2952(99)00152-5 | url = }}</ref> It was an [[receptor antagonist|antagonist]] or very weak partial agonist of the [[β3-adrenergic receptor|β<sub>3</sub>-adrenergic receptor]] (K<sub>act</sub> = {{Abbr|ND|not determined (due to low intrinsic activity)}}; {{Abbr|IA|Intrinsic activity}} = 7%).<ref name="VansalFeller1999" /> It is about 30,000 to 40,000{{nbsp}}times less potent as a β-adrenergic receptor agonist than [[isoproterenol|(–)-isoproterenol]].<ref name="VansalFeller1999" />

Pseudoephedrine's principal mechanism of action relies on its action on the adrenergic system.<ref name="American Medical Association, AMA Department of Drugs 1977 627">{{cite book| author = American Medical Association, AMA Department of Drugs|title=AMA Drug Evaluations|date=1977|publisher=PSG Publishing Co., Inc.|page=627}}</ref><ref name="Thomson/Micromedex 2007 2452">{{cite book| publisher = Thomson/Micromedex|title=Drug Information for the Health Care Professional | volume = 1 |date= 2007 |location=Greenwood Village, Colorado.|page=2452}}</ref> The [[vasoconstriction]] that pseudoephedrine produces is believed to be principally an α-adrenergic receptor response.<ref name='drew'>{{cite journal | vauthors = Drew CD, Knight GT, Hughes DT, Bush M | title = Comparison of the effects of D-(-)-ephedrine and L-(+)-pseudoephedrine on the cardiovascular and respiratory systems in man | journal = British Journal of Clinical Pharmacology | volume = 6 | issue = 3 | pages = 221–225 | date = September 1978 | pmid = 687500 | pmc = 1429447 | doi = 10.1111/j.1365-2125.1978.tb04588.x }}</ref> Pseudoephedrine acts on α- and β<sub>2</sub>-adrenergic receptors, to cause vasoconstriction and relaxation of smooth muscle in the bronchi, respectively.<ref name="American Medical Association, AMA Department of Drugs 1977 627"/><ref name="Thomson/Micromedex 2007 2452"/> α-Adrenergic receptors are located on the muscles lining the walls of blood vessels. When these receptors are activated, the muscles contract, causing the blood vessels to constrict (vasoconstriction). The constricted blood vessels now allow less fluid to leave the blood vessels and enter the nose, throat, and sinus linings, which results in decreased inflammation of nasal membranes, as well as decreased mucus production. Thus, by constriction of blood vessels, mainly those located in the nasal passages, pseudoephedrine causes a decrease in the symptoms of nasal congestion.<ref name="Eccles2007" /> Activation of β<sub>2</sub>-adrenergic receptors produces relaxation of the smooth muscle of the bronchi,<ref name="American Medical Association, AMA Department of Drugs 1977 627"/> causing bronchial dilation and in turn decreasing congestion (although not fluid) and difficulty breathing.

Pseudoephedrine is less [[potency (pharmacology)|potent]] as a sympathomimetic and [[psychostimulant]] than [[ephedrine]].<ref name="GłowackaWiela-Hojeńska2021" /><ref name="HughesEmpeyLand1983">{{cite journal | vauthors = Hughes DT, Empey DW, Land M | title = Effects of pseudoephedrine in man | journal = J Clin Hosp Pharm | volume = 8 | issue = 4 | pages = 315–321 | date = December 1983 | pmid = 6198336 | doi = 10.1111/j.1365-2710.1983.tb01053.x | url = | doi-access = free }}</ref> Clinical studies have found that pseudoephedrine is about 3.5- to 4-fold less potent than ephedrine as a sympathomimetic agent in terms of [[blood pressure]] increases and 3.5- to 7.2-fold or more less potent as a [[bronchodilator]].<ref name="HughesEmpeyLand1983" /> Pseudoephedrine is also said to have much less central effect than ephedrine and to be only a weak psychostimulant.<ref name="ODonnell1995" /><ref name="HughesEmpeyLand1983" /><ref name="Eccles2007" /><ref name="Abraham2003" /><ref name="AkibaSatohMastumura1982">{{cite journal | vauthors = Akiba K, Satoh S, Matsumura H, Suzuki T, Kohno H, Tadano T, Kisara K | title = [Effect of d-pseudoephedrine on the central nervous system in mice] | language = Japanese | journal = Nihon Yakurigaku Zasshi | volume = 79 | issue = 5 | pages = 401–408 | date = May 1982 | pmid = 6813205 | doi = 10.1254/fpj.79.401| url = }}</ref> [[Blood vessel]]s in the nose are around five times more sensitive than the [[heart]] to the actions of circulating [[epinephrine]] (adrenaline), which may help to explain how pseudoephedrine at the low doses used in over-the-counter products can produce nasal decongestion with minimal effects on the heart.<ref name="Eccles2007" /> Compared to [[dextroamphetamine]], pseudoephedrine is about 30 to 35{{nbsp}}times less potent as a norepinephrine releasing agent and 80 to 350{{nbsp}}times less potent as a [[dopamine releasing agent]] ''[[in vitro]]''.<ref name="RothmanVuPartilla2003" /><ref name="RothmanBaumannDersch2001" /><ref name="BaumannPartillaLehner2013" />

Pseudoephedrine is a very weak [[reversible inhibitor]] of [[monoamine oxidase]] (MAO) ''in vitro'', including both [[MAO-A]] and [[MAO-B]] (K<sub>i</sub> = 1,000–5,800{{nbsp}}μM).<ref name="UlusMaherWurtman2000">{{cite journal | vauthors = Ulus IH, Maher TJ, Wurtman RJ | title = Characterization of phentermine and related compounds as monoamine oxidase (MAO) inhibitors | journal = Biochem Pharmacol | volume = 59 | issue = 12 | pages = 1611–1621 | date = June 2000 | pmid = 10799660 | doi = 10.1016/s0006-2952(00)00306-3 | url = }}</ref> It is far less potent in this action than other agents like dextroamphetamine and [[moclobemide]].<ref name="UlusMaherWurtman2000" />

===Pharmacokinetics===
====Absorption====
Pseudoephedrine is [[oral administration|orally active]] and is readily [[absorption (pharmacokinetics)|absorbed]] from the [[gastrointestinal tract]].<ref name="GłowackaWiela-Hojeńska2021" /><ref name="Eccles2007" /> Its oral [[bioavailability]] is approximately 100%.<ref name="BruntonLazoParker2006" /> The drug reaches [[Cmax (pharmacology)|peak]] concentrations after 1 to 4{{nbsp}}hours (mean 1.9{{nbsp}}hours) in the case of the [[immediate-release]] formulation and after 2 to 6{{nbsp}}hours in the case of the [[extended-release]] formulation.<ref name="GłowackaWiela-Hojeńska2021" /><ref name="Eccles2007" /> The [[onset of action]] of pseudoephedrine is 30{{nbsp}}minutes.<ref name="GłowackaWiela-Hojeńska2021" />

====Distribution====
Pseudoephedrine, due to its lack of [[Chemical polarity|polar]] [[Phenols|phenolic]] [[functional group|group]]s, is relatively [[lipophilic]].<ref name="ChuaBenrimojTriggs1989" /> This is a property it shares with related sympathomimetic and decongestant agents like [[ephedrine]] and [[phenylpropanolamine]].<ref name="ChuaBenrimojTriggs1989" /> These agents are widely [[distribution (pharmacology)|distributed]] throughout the body and cross the [[blood–brain barrier]].<ref name="ChuaBenrimojTriggs1989" /> However, it is said that pseudoephedrine and phenylpropanolamine cross the blood-brain barrier only to some extent and that pseudoephedrine has limited [[central nervous system]] activity, suggesting that it is partially [[peripherally selective drug|peripherally selective]].<ref name="ODonnell1995" /><ref name="BouchardWeberGeiger2002" /> The blood-brain barrier permeability of pseudoephedrine, ephedrine, and phenylpropanolamine is reduced compared to other [[substituted amphetamine|amphetamines]] due to the presence of a [[hydroxyl group]] at the β carbon which decreases their [[lipophilicity]].<ref name="BouchardWeberGeiger2002">{{cite journal | vauthors = Bouchard R, Weber AR, Geiger JD | title = Informed decision-making on sympathomimetic use in sport and health | journal = Clin J Sport Med | volume = 12 | issue = 4 | pages = 209–224 | date = July 2002 | pmid = 12131054 | doi = 10.1097/00042752-200207000-00003 | url = }}</ref> As such, they have a greater ratio of peripheral cardiovascular to central psychostimulant effect.<ref name="BouchardWeberGeiger2002" /> Besides entering the brain, these substances also cross the [[placenta]] and enter [[breast milk]].<ref name="ChuaBenrimojTriggs1989" />

The [[plasma protein binding]] of pseudoephedrine has been reported to be approximately 21 to 29%.<ref name="VolppHolzgrabe2019" /><ref name="Schmidt2023" /> It is bound to [[orosomucoid|α<sub>1</sub>-acid glycoprotein]] (AGP) and [[human serum albumin|albumin]] (HSA).<ref name="VolppHolzgrabe2019" /><ref name="Schmidt2023" />

====Metabolism====
Pseudoephedrine is not extensively [[drug metabolism|metabolized]] and is subjected to minimal [[first-pass metabolism]] with oral administration.<ref name="ChuaBenrimojTriggs1989" /><ref name="GłowackaWiela-Hojeńska2021" /><ref name="Eccles2007" /> Due to its [[methyl group]] at the α [[carbon]] (i.e., it is an [[substituted amphetamine|amphetamine]]), pseudoephedrine is not a [[substrate (biochemistry)|substrate]] for [[monoamine oxidase]] (MAO) and is not metabolized by this [[enzyme]].<ref name="ODonnell1995" /><ref name="ChuaBenrimojTriggs1989" /><ref name="JohnsonHricik1993">{{cite journal | vauthors = Johnson DA, Hricik JG | title = The pharmacology of alpha-adrenergic decongestants | journal = Pharmacotherapy | volume = 13 | issue = 6 Pt 2 | pages = 110S–115S; discussion 143S–146S | date = 1993 | pmid = 7507588 | doi = 10.1002/j.1875-9114.1993.tb02779.x| url = }}</ref><ref name="Broadley2010" /> It is also not metabolized by [[catechol O-methyltransferase|catechol ''O''-methyltransferase]] (COMT).<ref name="ODonnell1995" /> Pseudoephedrine is [[demethylation|demethylated]] into the [[metabolite]] [[cathine|norpseudoephedrine]] to a small extent.<ref name="GłowackaWiela-Hojeńska2021" /><ref name="ChuaBenrimojTriggs1989" /> Similarly to pseudoephedrine, this metabolite is [[active metabolite|active]] and shows [[amphetamine]]-like effects.<ref name="ChuaBenrimojTriggs1989" /> Approximately 1 to 6% of pseudoephedrine is metabolized in the [[liver]] via ''N''-demethylation to form norpseudoephedrine.<ref name="GłowackaWiela-Hojeńska2021" />

====Elimination====
Pseudoephedrine is [[excretion|excreted]] primarily via the [[kidney]]s in [[urine]].<ref name="GłowackaWiela-Hojeńska2021" /><ref name="ChuaBenrimojTriggs1989" /> Its urinary excretion is highly influenced by urinary [[pH]] and is increased when the urine is [[acidic]] and is decreased when it is [[alkaline]].<ref name="GłowackaWiela-Hojeńska2021" /><ref name="ChuaBenrimojTriggs1989" /><ref name="HughesEmpeyLand1983" />

The [[elimination half-life]] of pseudoephedrine on average is 5.4{{nbsp}}hours<ref name="Eccles2007" /> and ranges from 3 to 16{{nbsp}}hours depending on urinary pH.<ref name="GłowackaWiela-Hojeńska2021" /><ref name="ChuaBenrimojTriggs1989" /> At a pH of 5.6 to 6.0, the [[elimination half-life]] of pseudoephedrine was 5.2 to 8.0{{nbsp}}hours.<ref name="ChuaBenrimojTriggs1989" /> In one study, a more acidic pH of 5.0 resulted in a half-life of 3.0 to 6.4{{nbsp}}hours, whereas a more alkaline pH of 8.0 resulted in a half-life of 9.2 to 16.0{{nbsp}}hours.<ref name="ChuaBenrimojTriggs1989" /> Substances that influence urinary acidity and are known to affect the excretion of amphetamine derivatives include [[acidifier|urinary acidifying agents]] like [[ascorbic acid]] and [[ammonium chloride]] as well as [[alkalinizing agent|urinary alkalinizing agents]] like [[acetazolamide]].<ref name="PatrickMarkowitz1997"/>

A majority of an [[oral administration|oral]] dose of pseudoephedrine is excreted unchanged in urine within 24{{nbsp}}hours of administration.<ref name="ChuaBenrimojTriggs1989" /> This has been found to range from 43 to 96%.<ref name="GłowackaWiela-Hojeńska2021" /><ref name="ChuaBenrimojTriggs1989" /><ref name="Eccles2007" /> The amount excreted unchanged is dependent on urinary pH similarly to the drug's half-life, as a longer half-life and duration in the body allows more time for the drug to be metabolized.<ref name="ChuaBenrimojTriggs1989" />

The [[duration of action]] of pseudoephedrine, which is dependent on its [[elimination (pharmacology)|elimination]], is 4 to 12{{nbsp}}hours.<ref name="GłowackaWiela-Hojeńska2021" /><ref name="Aaron1990" />

Pseudoephedrine has been reported to accumulate in people with [[renal impairment]].<ref name="Sequeira1998">{{cite book | vauthors = Sequeira RP N| title=Side Effects of Drugs Annual | chapter=Central nervous system stimulants and drugs that suppress appetite | publisher=Elsevier | volume=21 | date=1998 | isbn=978-0-444-82818-7 | doi=10.1016/s0378-6080(98)80005-6 | pages=1–8}}</ref><ref name="SicaComstock1989">{{cite journal | vauthors = Sica DA, Comstock TJ | title = Pseudoephedrine accumulation in renal failure | journal = Am J Med Sci | volume = 298 | issue = 4 | pages = 261–263 | date = October 1989 | pmid = 2801760 | doi = 10.1097/00000441-198910000-00010 | url = }}</ref><ref name="LyonTurney1996">{{cite journal | vauthors = Lyon CC, Turney JH | title = Pseudoephedrine toxicity in renal failure | journal = Br J Clin Pract | volume = 50 | issue = 7 | pages = 396–397 | date = 1996 | pmid = 9015914 | doi = 10.1111/j.1742-1241.1996.tb09584.x| url = }}</ref>